Friday, 25 May 2012

Are anthropogenic pressures increasing the speed of bacterial evolution?

It wasn't so long ago that antibacterial products, from soaps to hand gels to wipes for your kitchen counter, became ubiquitous in our grocery stores and our daily lives. Not long afterwards, though, we started hearing reports that these products and their even more powerful cousins, antibiotic prescriptions, were actually doing more harm than good--by facilitating the evolution of bacterial resistance to antimicrobials. As it turns out, that may be just be one evolutionary side effect of exposing bacteria to strongly selective anthropogenic pressures. An even more fundamentally important one is the ability to evolve rapidly, quickly incorporating genetic changes in order to display a different phenotype--in this case, increased or more comprehensive robustness in the face of antimicrobial treatments. This means that our struggles to deal with antibiotic-resistant strains, such as the dreaded methicillin-resistant Stapholococcus aureus (MRSA), are only just the tip of the iceberg.

The question of whether humans are increasing bacterial "evolvability" is addressed by two Australian researchers in a review article published in the latest issue of Trends in Ecology and Evolution. They define "evolvability" as "an increased potential for evolution," which can be driven by characteristics such as basal mutation rate, recombination rates, protection against the incorporation of foreign DNA into the genome, and propensity for lateral gene transfer (or acquiring genes from a source other than a "parent"). All of these traits "affect the rate at which genetic variation can be generated"--and some of this variation could very well confer resistance.

Interestingly, many antibiotics were originally isolated from soil
bacteria, which probably developed these compounds for use in signalling
or competition with neighbors. For cells to survive in these
potentially toxic environments, they had to evolve resistance genes
alongside those producing poison, and so the terrestrial environment is
probably already teeming with genetic elements offering protection from
various man-made drugs. Once our antibiotic runoff reaches these
environments, bacteria without the genes die off, while those with them
will survive, passing on the resistance not only to their "offspring"
but also, potentially, to their neighbors. Cells with higher levels of
evolvability will become resistant more quickly; in other words,
exposure to antibiotics leads not only to the selection of resistance,
but also of the ability to develop it. This process works so well that
the number of antibiotic-resistant genetic elements has increased
significantly over the years. Many such elements are located in wild
animals or environments not directly exposed to antibiotics, strongly
suggesting that resistance has spread along a bacterial supply chain
that begins in anthropogenic environments and extends even into those
otherwise considered "pristine."

The authors point out that evolvability is not always a useful characteristic for bacteria to possess. For instance, while some mutations can be advantageous, others can impair functionality or even remove it altogether; likewise, incorporation of DNA from an unrelated bacterium might result in the transcription of a useful protein, but it also could generate something that is ultimately toxic. Thus, we should expect evolvability to be high only in systems where it's a gamble that, more often than not, pays off. This describes the current state of affairs in both terrestrial and aquatic ecosystems, into which humans dump vast quantities of antibiotics each year--especially in the form of waste water. The exact amounts are difficult to measure, but are likely to be large if they are even a small portion of the millions of metric tons produced annually.

(Acinetobacter baumannii, a gram-negative bacterium that is sometimes known as "Iraqibacter" because of its prevalence among US soldiers wounded to Iraq.)

One particularly frightening aspect of the spread of resistance is how it can often involve whole suites of genes rather than just one. Acinetobacter baumannii, for instance, now possesses a "resistance island" containing 45 genes for antibiotic/antimicrobial resistance, as well as resistance to heavy metals such as mercury and arsenic. As a result, A. baumannii infections have become a much greater threat to human health over the last several decades; additionally, these bacteria have given rise to a number of new hybrids and variants that are also likely to cause trouble in the future. Indeed, higher levels of evolvability are likely not only to increase the threat from current pathogens, but also "stimulate the emergence of new disease agents" from organisms that used to be our friendly neighbors.

As mentioned earlier, however, evolvability should be found at relatively lower levels in systems where it leads to more harm than good--for instance, places where there is limited exposure to novel antibiotic products. It is unlikely that we will be able to easily remove current contamination, but we can limit the amount introduced in the future by minimizing unnecessary use of antimicrobials and by disposing of them in a more eco-friendly way. This won't stop bacteria from developing defenses against our drugs and disinfectants, but it might help reduce the speed with which they do so.

Who is the "Anthrophysist"?

I am a biologist who studies the ways in which anthropogenic disturbance impacts animals (especially birds). I hope that the results of my work, and the work of other researchers like me, can help humans learn how to coexist more peacefully with wildlife. I am also interested in the role that nature has played in shaping human cultures around the world and over the centuries. Although this blog will predominantly focus on scientific research, I hope to occasionally profile some anthropological work as well, in order to better highlight the interconnectedness of humans ("anthro") and nature ("physis").